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Article

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells.

Nature communications - 27 Jul 2024

Ramakrishnan Natasha, Weaver Tyler M, Aubuchon Lindsey N, Woldegerima Ayda, Just Taylor, Song Kevin, Vindigni Alessandro, Freudenthal Bret D, Verma Priyanka

Abstract excerpt

Clinical success with poly (ADP-ribose) polymerase inhibitors (PARPi) is impeded by inevitable resistance and associated cytotoxicity. Depletion of Amplified in Liver Cancer 1 (ALC1), a chromatin-remodeling enzyme, can overcome these limitations by hypersensitizing BReast CAncer genes 1/2 (BRCA1/2) mutant cells to PARPi. Here, we demonstrate that PARPi hypersensitivity upon ALC1 loss is reliant on its role in...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to DNA-(Apurinic or Apyrimidinic Site) Lyase

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Source

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Identifiers

PMID: 39068174
DOI: 10.1038/s41467-024-50673-7
PMCID: PMC11283519

Genes

BRCA1
PARP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells.PMID 39068174Read ↗

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